One hundred six patients with terminal renal insufficiency and 29 medical personnel were given three doses of hepatitis B vaccine at an interval of 0, 1, and 6 months (Merck, Sharp and Dohme, West Point, Pennsylvania, part of a joint study no. 649). Chronic hemodialysis patients (N = 99) received 40 micrograms vaccine (V) i.m. Uremic patients, who were just about to start chronic dialysis treatment (N = 7), were given 40 micrograms V, and at the first vaccination 3 ml hyperimmune globulin (HBIG) in addition. The medical personnel was alternately vaccinated with 20 micrograms V (N = 8), 40 micrograms (N = 11), 40 micrograms V, and 3 ml HBIG at the first vaccination (N = 10). After 12 months, 50% of the male dialysis patients, 66% of the female dialysis patients, and 95% of the medical staff developed anti-HBs antibodies. The anti-HBs titer of the dialysis patients was ten times lower than in the medical staff. The simultaneous passive immunization did not lead to any impairment of the anti-HBs titer in the dialysis patients and staff. The type of renal disease, length of time on dialysis, hematocrit, and immunoglobulin concentration did not influence the rate of immunization. After 12 months, 43 patients without antibody response were vaccinated a fourth time. Sixteen of these patients then developed anti-HBs, improving the immunization rate from 56.5 to 71.7%. A fifth vaccination only led to seroconversion, when brief or borderline anti-HBs could already be demonstrated previously. In dialysis patients who fail to develop anti-HBs after three doses of vaccine, a fourth vaccination is recommended after 12 months.

No abstract

Eighty-eight asymptomatic carriers of hepatitis B surface antigen (HBsAg) were followed with biochemical, serologic, histologic, and immunohistologic studies over a period of four years. None of the 78 HBsAg carriers with normal or minimally changed liver tissue, antibody to hepatitis B e antigen (HBeAg) in serum, and no intranuclear hepatitis B core antigen (HBcAg) developed a chronic inflammatory liver disease. Four individuals lost circulatory HBsAg, and at least two individuals terminated their HBsAg carrier state. Seven asymptomatic HBsAg carriers with chronic hepatitis were characterized by HBeAg in serum and intranuclear HBcAg. However, three HBsAg carriers with chronic hepatitis and an absence of intrahepatocellular HBcAg were positive for antibody to HBeAg over the observation period. The mechanism that leads to chronic hepatitis in these patients remains to be determined.